The present invention pertains to implantable medical devices (IMDs), particularly gastrointestinal stimulator and/or monitor IMDs adapted to be implanted within the interior of the gastrointestinal tract having one or more than one stimulation/sense electrode attached to or pressing against an interior surface site of the gastrointestinal tract wall to conduct electrical stimulation to the site and to conduct electrical signals of the GI tract from the site or other physiologic signals from the interior of the gastrointestinal tract.
The GI tract comprises the esophagus, the stomach, the small intestine, the large intestine, the colon, and the anal sphincter and is generally described as having a tract axis. Like other organs of the body, most notably the heart, these organs naturally undergo regular rhythmic contractions. In particular these contractions take the form of peristaltic contractions and are essential for the movement of food through each of the respective organs. Like the heart, these contractions are the result of regular rhythmic electrical depolarizations of the underlying tissue.
In some individuals, however, either the regular rhythmic peristaltic contractions do not occur or the regular rhythmic electrical depolarizations do not occur or both do not occur. In each of these situations the movement of food may be seriously inhibited or even disabled. Such a condition is often called xe2x80x9cgastroparesisxe2x80x9d when it occurs in the stomach. Gastroparesis is a chronic gastric motility disorder in which there is delayed gastric emptying of solids or liquids or both. Symptoms of gastroparesis may range from early satiety and nausea in mild cases to chronic vomiting, dehydration, and nutritional compromise in severe cases. Similar motility disorders occur in the other organs of the GI tract, although by different names.
Diagnosis of gastroparesis is based on-demonstration of delayed gastric emptying of a radio-labeled solid meal in the absence of mechanical obstruction. Gastroparesis may occur for a number of reasons. Management of gastroparesis involves four areas: (1) prokinetic drugs, (2) antiemetic drugs, (3) nutritional support, and (4) surgical therapy (in a very small subset of patients.) Gastroparesis is often a chronic, relapsing condition; 80% of patients require maintenance antiemetic and prokinetic therapy and 20% require long-term nutritional supplementation. Other maladies such as tachygastria or bradygastria can also hinder coordinated muscular motor activity of the GI tract, possibly resulting in either stasis or nausea or vomiting or a combination thereof.
The undesired effect of these conditions is a reduced ability or complete failure to efficiently propel intestinal contents down the digestive tract. This results in malassimilation of liquid or food by the absorbing mucosa of the intestinal tract. If this condition is not corrected, malnutrition or even starvation may occur. Moreover nausea or vomiting or both may also occur. Whereas some of these disease states can be corrected by medication or by simple surgery, in most cases treatment with drugs is not adequately effective, and surgery often has intolerable physiologic effects on the body.
The concept of electrically stimulating the gastrointestinal tract to restore its proper function originated many years ago, and one early approach is disclosed in commonly assigned U.S. Pat. No. 3,411,507. The ""507 patent discloses a system for gastrointestinal stimulation which uses an electrode positioned on a nasogastric catheter and an electrode secured to the skin over the abdomen. In operation, the nasogastric catheter is inserted into the patient""s stomach while the patient is lying down such that the electrode is positioned in close proximity to the pylorus of the stomach. Electrical stimulation is delivered for the first five seconds of every minute until peristaltic activity is initiated. The ""507 patent also discloses using electrical stimulation of the same order of magnitude as the normal range of periodicity of the inherent peristaltic pacemaker action of the duodenum. The stimulation process is discontinued after the first bowel movement. The ""507 patent system is a short-term device that is only useful for patients in a hospital setting, and particularly non-ambulatory patients.
Sensing of the peristaltic electrical wave and gastrointestinal stimulation at various sites on or in the GI tract wall of the digestive system or nerves associated therewith have been conducted to diagnose and treat these various conditions over the years since the publication of the ""507 patent. Fully implantable gastrointestinal stimulation systems have been developed and clinically implanted in patient""s bodies allowing the patients to be ambulatory. The history and breadth of such sensing and GI tract stimulation is set forth in commonly assigned U.S. Pat. Nos. 5,507,289, 6,026,326, 6,104,965, 6,216,039, and in further U.S. Pat. Nos. 5,690,691 and 6,243,607, for example. The implantable gastrointestinal stimulation systems are referred to as xe2x80x9cpacemakersxe2x80x9d in certain of these patents and the literature because of their resemblance to implantable cardiac pacemakers in structure and function.
In such fully implantable gastrointestinal stimulation systems, electrical stimuli are applied from an implantable pulse generator (IPG) through elongated leads and lead borne electrodes affixed at sites in the body of the patient or the GI tract wall or the vagus nerve that permit the electrical stimulus to produce a local contraction of a desired portion of the GI tract. The IPG is typically implanted below the skin surface in the abdominal region and leads coupled to the IPG extend to sites of the gastrointestinal tract and/or the vagus nerve where stimulation/sense electrodes are affixed.
The sites of the GI tract wall typically comprise the outermost serosa or sub-serosally in the inner, circumferential and longitudinal (and oblique in the case of the stomach) smooth muscle layers referred to as the xe2x80x9cmuscularis externaxe2x80x9d (although the above referenced ""691 patent suggests locating the electrodes within the stomach cavity against the inner stomach surface mucosa). The above-referenced ""607 patent discloses one method and system for electrical stimulation of smooth muscle with intact local gastric nerves comprising a portion of the GI tract. The electrical stimulation of the smooth muscle effects local contractions at sites of a portion of the GI tract that are artificially propagated distally therethrough in order to facilitate or aid at least a partial emptying of such portion. This stimulation attempts to create a simulated system that reproduces the spatial and temporal organization of normal gastric electrical activity by creating and controlling local circumferential non-propagated contractions. In this simulated gastric pacing system, each local circumferential contraction is invoked by applying an electrical stimulus to the smooth muscle circumferentially about the portion of the GI tract in a plane substantially perpendicular to the longitudinal axis of the portion. The electrical stimulus is applied at a proximal location and at least one distal location. The distal location is in axially spaced relationship relative to the proximal location. Further, the applied electrical stimulus is selected to be sufficient to stimulate the smooth muscle to produce the local circumferential contractions at the proximal and distal locations.
The Medtronic(copyright) Itrel III(copyright) Model 7425 IPG and pairs of the unipolar Model 4300 or Model 4301 or Model 4351 xe2x80x9csingle passxe2x80x9d leads available from MEDTRONIC, INC. have been implanted to provide stimulation to sites in the stomach wall to treat chronic nausea and vomiting associated with gastroparesis. The unipolar electrode of these leads comprises a length of exposed lead conductor and is of the type disclosed in commonly assigned U.S. Pat. Nos. 5,425,751, 5,716,392 and 5,861,014. The above-referenced ""039 patent and the ""014 patent disclose the Model 4300 lead sewn through the serosa laterally into the muscularis externa to dispose the stimulation/sense electrode therein. A large incision is necessary to access the site, and a needle is used to perforate the serosa and muscularis externa laterally without fully penetrating the wall and to draw the stimulation/sense electrode into the muscularis externa. A laparascopic approach can be taken, but it is difficult to maneuver the needle to effect the fixation of the stimulation/sense electrode at the site. It is suggested in the ""039 patent that two or more electrodes of this type can be formed along the length of the lead body that would be sewn laterally through and disposed within the muscularis externa.
A further U.S. Pat. No. 5,292,394 discloses a percutaneous system that provides for temporary stimulation, sensing, delivery of fluids and nutrients, and pH sensing within the gastrointestinal tract. A plurality of distal stimulation/sense electrodes are located within the stomach cavity pressing against the mucosa, and distal pressure and pH sensors are located in the stomach cavity and the small intestine. The sensors and stimulation/sense electrodes are electrically coupled to an external pulse generator/controller by lead conductors extending through a percutaneously introduced access device or tube that the distal components were introduced through. Fluids can also be introduced directly into the stomach or withdrawn from the stomach. The percutaneous pathway is problematic in that the seal around the percutaneous access device that is necessary to prevent leakage of stomach acid into the peritoneal cavity or just subcutaneously around the device.
Ways of attaching pH sensors within the esophagus via the patient""s mouth employing an endoscope are disclosed in U.S. Pat. No. 6,258,896. The attachment embodiments disclosed in the ""896 patent include use of a loop drawn about a mass of mucosal tissue, a tether tied to a tooth in the patient""s mouth, and a recital of the use of hooks, barbs, sutures, tacks, staples, other structures that penetrate the mucosa. It is also suggested that the fixation mechanism be made biodegradable so that the biosensor capsule would be released after a monitoring time period and pass through the GI tract.
Ways of attaching pH sensors within the stomach via the mouth employing an endoscope are disclosed in an article by Swain et al. entitled xe2x80x9cAn endoscopically deliverable tissue-transfixing device for securing biosensors in the gastrointestinal tractxe2x80x9d, GASTOINTESTINAL ENDOSCOPY vol. 40, no. 6, pp. 730-734, 1994. The attachment mechanism involves use of suction to draw a fold of the stomach wall together and insertion of a preformed, Nylon, H-shaped tag through the fold of the stomach wall. While pH sensors are described, it is suggested that the same equipment and fixation mechanism can be employed to fix other medical devices within the stomach, including xe2x80x9celectrical pacemakersxe2x80x9d, presumably to stimulate the stomach wall. No specific sensing or stimulation electrodes are described.
In the field of cardiac stimulation, cardiac pacing leads having bipolar and unipolar pace/sense electrodes have long been used in conjunction with pacing system IPGs to conduct pacing pulses generated by the IPG to a site of the heart and cardiac signals from the site to the IPG. Pacing leads are typically provided with a passive fixation or an active fixation mechanism at the lead body distal end that is passively or actively engaged with cardiac tissue to anchor a distal tip electrode at a desired site in or on the heart. Passive fixation generally involves an atraumatic fixation lodging the distal electrode against the endocardium or within a coronary blood vessel. Positive or active fixation generally involves a more traumatic penetration of a fixation mechanism into the myocardium from an endocardial or epicardial surface, and the active fixation mechanism commonly comprises a distal pace/sense electrode. Typically, the active fixation mechanism comprises the single pace/sense electrode or one of the bipolar pace/sense electrodes, but can be separate and electrically isolated from the pace/sense electrodes.
Endocardial pacing leads having either active fixation or passive fixation mechanisms are implanted by a transvenous route into a heart chamber to locate the distal pace/sense electrode(s) at a selected site in the heart chamber where an active or passive fixation mechanism is deployed to maintain the pace/sense electrode affixed at the site. Endocardial active fixation pacing leads typically employ extendable and retractable helixes of hooks that are retracted during introduction and are extended distally from the lead body distal end at the site of attachment.
Epicardial pacing leads are implanted by exposure of the epicardium of the heart through a limited thoracotomy. The distal end of the epicardial lead formed with one or two pace/sense electrodes and an active fixation mechanism supported by an electrode head is affixed through the epicardium and within the myocardium. Active fixation mechanisms of epicardial pacing leads typically comprise a tissue penetrating, self-affixing mechanism extending away from a support or base or plate of the electrode head. The fixation mechanism is forced into the myocardium typically employing an insertion tool engaging the electrode head until it is fully seated within the myocardium and the plate bears against the epicardium. The plate is typically formed with a tissue ingrowth encouraging fabric or lattice, whereby tissue ingrowth about the plate assists in chronic anchoring to the heart.
The dislodgement of pace/sense electrodes and the fracture of the lead conductor or the insulation about it were serious concerns in the early years of implantable cardiac pacemakers. A combined pacemaker IPG, pace/sense electrodes, and active fixation barb mechanism are disclosed in U.S. Pat. No. 3,835,864 that is intended to overcome the problems associated with lead fracture and electrode dislodgement. A system and method are disclosed for introducing the unitary pacemaker through a transvenous route, lodging it deeply in the right ventricular apex, and deploying the active fixation barbs. Other implantation sites are suggested, including in relation to sphincters, but no particular examples of the implantation are described. The disclosed unitary pacemaker has not been clinically implanted in humans.
To our knowledge, none of the above-described medical devices have been employed in the field of gastrointestinal stimulation. There remains a need to provide an implantable GI tract stimulator for providing GI tract electrical stimulation at sites in the stomach that can be introduced into the stomach cavity and affixed to the stomach wall without an invasive surgical procedure, that is simple to affix at a desired site, that is securely affixed for temporary or chronic stimulation, and that can be removed when necessary.
The present invention is preferably embodied in a GI tract stimulator or monitor IMD that can be introduced through the esophagus, that is simple to affix to the stomach or GI tract wall at a desired site, that is securely affixed thereto, and that can be removed when necessary. The IMD is preferably a GI tract stimulator and/or a physiologic signal monitor.
The GI tract stimulator or monitor of the present invention comprises a hermetically sealed housing enclosing electrical stimulation and/or monitoring circuitry and a power source and an elongated flexible member extending from the housing to an active fixation mechanism adapted to be fixed into the mucosa or sub-mucosal tissue. After fixation is effected, the elongated flexible member bends into a preformed shape that presses the housing against the mucosa so that forces that would tend to dislodge the fixation mechanism are minimized.
Preferably, a GI tract stimulator or monitor IMD in accordance with the present invention comprises a hermetically sealed housing enclosing electrical stimulation and/or monitoring circuitry and a power source and supporting a first stimulation/sense electrode adapted to press against the mucosa of the stomach wall. An elongated flexible member is fixed at a member fixed end to the housing and extends away from the housing to a member free end supporting an active fixation mechanism and a second stimulation/sense electrode. The active fixation mechanism is adapted to grip a fold of the mucosa or perforate the mucosa and lodge in the muscularis externa of the GI tract wall when introduced against the mucosa. The active fixation mechanism and second stimulation/sense electrode can be separately supported at the member free end or combined together. A conductor is encased within or extends through a first lumen of the flexible member and is coupled to the second stimulation/sense electrode and to the IPG circuitry within the hermetically sealed housing.
The flexible member is formed to assume a bend intermediate the member fixed end and the member free end when the flexible member is unrestrained. However, the flexible member can be straightened to axially align and enable the introduction of the straightened flexible member and hermetically sealed housing through the lumen of an esophageal catheter. Preferably, an elongated beam of shape memory alloy having the bend formed in it is encased within or extends through a second lumen of the flexible member.
In use, the GI tract stimulator or monitor IMD is fitted into the lumen of an esophageal tube or catheter with the fixation mechanism aimed toward the catheter distal end opening whereby the bend in the flexible member is straightened and the fixation mechanism is contained within the catheter lumen. The catheter (and endoscope) is inserted through a curved mouth and throat guard inserted into the patient""s mouth, and the catheter distal end is advanced through the esophagus and lower esophageal sphincter and into the stomach cavity. An endoscope can also be inserted through the catheter lumen or alongside the esophageal catheter to enable visualization of the stomach wall to locate a fixation site and to observe the fixation. The catheter distal end is directed to the site of implantation
The fixation mechanism is then deployed to fix the flexible member free end to the stomach wall. The fixation mechanism can be any of those employed to fix IMDs in the body. Preferred forms of fixation mechanisms comprise a helix, one or more hook, or clips or pincers that penetrate through the mucosa into the muscularis externa or pinch a fold of the mucosa. The mucosa can be drawn against the esophageal catheter distal end by drawing suction through the catheter lumen. The fixation mechanism is then pushed or screwed into the stomach wall or the clip or pincers are released to engage the stomach wall fold.
Then, the esophageal catheter is withdrawn to release the GI tract stimulator, whereupon the flexible member assumes its bent configuration and lodges the hermetically sealed housing against the mucosa. The first stimulation/sense electrode is preferably an exposed conductive portion of the housing that is aligned with the bend of the flexible member so that it is pressed against the mucosa.
For temporary use, the fixation mechanism can be made of a material that is degraded by stomach acid over time to release the GI tract stimulator or monitor IMD and allow it to pass through the GI tract. Alternatively, the removal can be effected by straightening the bend and withdrawing the GI tract stimulator or monitor IMD through the lumen of an esophageal catheter introduced in the same way into the stomach. A wire can be advanced through the catheter lumen to snare or otherwise engage the GI tract stimulator and draw it into the catheter lumen.
The active fixation mechanisms preferably extend away from a stop or plate of the electrode head and are shaped to penetrate through the mucosa and into the muscularis externa upon application of penetrating force through the electrode head to the GI tract wall to draw the stop or plate against the mucosa and operatively contact the stimulation/sense electrode with the GI tract wall. The stop or plate inhibits further advancement of the active fixation mechanism and perforation of the GI tract wall, and the active fixation mechanism cooperates with the stop or plate to inhibit dislodgement of the stimulation/sense electrode from operative contact with the GI tract wall.
The active fixation mechanisms are selected from helixes and barbed hooks having sharpened tips or free ends that perforate the mucosa and lodge in the muscularis externa or the submucosa. The maximal depth of penetration from the stop or plate is preferably in the range of 1 mm to 15 mm when the site comprises the antrum or in the range of 1 mm to 10 mm when the site comprises corpus or fundus to ensure that the free end does not extend substantially through the stomach wall.
The helixes and hooks can be formed of bio-compatible conductive materials that are coupled with the lead conductors and un-insulated at least in part to operate as the sensing and/or stimulation electrodes. The stimulation/sense electrode surface can be coated with a porous platinized structure to reduce polarization and/or an anti-inflammatory agent that inhibits inflammation that can negatively affect the ability to sense electrical signals of the GI tract or to efficiently deliver electrical stimulation. The anti-inflammatory agents can be embedded into a monolithic controlled release device (MCRD) carried by the electrode head.
The expression xe2x80x9cstimulation/sense electrodexe2x80x9d as used herein applies to stimulation electrodes that are employed to stimulate tissue or sense electrodes to sense electrical signals in the tissue or electrodes that are used to perform both functions.
This summary of the invention has been presented here simply to point out some of the ways that the invention overcomes difficulties presented in the prior art and to distinguish the invention from the prior art and is not intended to operate in any manner as a limitation on the interpretation of claims that are presented initially in the patent application and that are ultimately granted.